Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 2,360

Circa 2016

Just lopped off your ring finger slicing carrots (some time in the future)? No problem. Just speed-read this article while you’re waiting for the dronebulance. …

“Epimorphic regeneration” — growing digits, maybe even limbs, with full 3D structure and functionality — may one day be possible. So say scientists at Tulane University, the University of Washington, and the University of Pittsburgh, writing in a review article just published in Tissue Engineering, Part B, Reviews (open access until March 8).

The process of amphibian epimorphic regeneration may offer hints for humans. After amputation, the wound heals to form an epidermal layer, the underlying tissues undergo matrix remodeling, and cells in the region secrete soluble factors. A heterogeneous cell mass, or blastema, forms from the proliferation and migration of cells from the adjacent tissues. The blastema then gives rise to the various new tissues that are spatially patterned to reconstruct the original limb structure. (credit: Lina M. Quijano et al./Tissue Engineering Part B)

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Regular infusions of an antibody that blocks the HIV binding site on human immune cells may have suppressed levels of HIV for up to four months in people undergoing a short-term pause in their antiretroviral therapy (ART) regimens, according to a report published online today in The New England Journal of Medicine. Results of the Phase 2, open-label study indicate the antibody, known as UB-421, was safe and did not induce the production of antibody-resistant HIV. The study was supported in part by the National Institute of Allergy and Infectious Diseases (NIAID), a component of the National Institutes of Health, and United Biopharma, Inc.

The study was conducted in Taiwan and led by Chang Yi Wang, Ph.D., Chief Scientific Officer and Chairperson of United BioPharma, Inc. Twenty-nine volunteers with well-controlled HIV discontinued their normal regimens of daily oral ART at the time of their first or one week later, depending on their ART regimen. Fourteen received eight regular weekly infusions of UB-421, while 15 received eight higher-dose infusions every other week. At the end of the 8- or 16-week treatment period, all volunteers restarted their previous ART regimen and were evaluated in follow-up visits up to eight weeks later. Apart from a single participant who discontinued the study because of a mild skin rash, volunteers in both groups maintained HIV suppression (plasma HIV RNA levels under 20 copies/mL) throughout the treatment period in the absence of ART.

Previous experimental infusions of broadly neutralizing antibodies, or bNAbs, have suppressed HIV for about two weeks by targeting proteins on the virus itself, but the rapid mutation rate of HIV induces antibody-resistant strains that render the treatment ineffective. UB-421 theoretically avoids this possibility by blocking a stable human protein that HIV uses to infect T cells. Indeed, resistance to UB-421 was not seen in this study. Because the small study did not include a comparator group receiving a placebo infusion, further studies have been planned in Taiwan and Thailand to evaluate the safety and efficacy of UB-421 as a treatment for HIV. In a related study, NIAID investigators currently are evaluating the safety of regular infusions of two highly potent bNAbs that may prevent the development of resistant HIV strains by targeting two distinct areas of the virus.

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Advanced pancreatic cancer is often symptomless, leading to late diagnosis only after metastases have spread throughout the body. Additionally, tumor cells are encased in a “protective shield,” a microenvironment conferring resistance to many cancer treatment drugs. Now, Salk Institute researchers, along with an international team of collaborators, have uncovered the role of a signaling protein that may be the Achilles’ heel of pancreatic cancer.

The findings, published in Nature on April 17, 2019, show that pancreatic —resident cells typically dormant in normal tissue—become activated and secrete proteins to form a shell around the in an attempt to wall off and contain it. The activated stellate cells also secrete a signaling protein called LIF, which conveys stimulatory signals to to drive pancreatic cancer development and progression. Results also suggest LIF may be a useful biomarker to help diagnose pancreatic cancer more quickly and efficiently.

“There haven’t been very many advances in pancreatic cancer therapy because it’s a difficult cancer to diagnose and treat,” says Salk American Cancer Society Professor Tony Hunter. “Understanding this communication network between the cancer cells and stellate cells may enable us to develop more effective therapies, along with tools for earlier diagnosis.”

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The results of a clinical trial using bone marrow-derived mesenchymal stromal cells (MSCs) to treat late-stage knee osteoarthritis were published recently, and they came back positive. The trial included both phase 1 and 2 and was designed to determine the safety and efficacy of MSC stem cell therapy.

A battery of tests

During the trial, patients were given a single injection of 1, 10, or 50 million MSCs directly into the knee. The trial used a number of tests associated with knee osteoarthritis, including the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), a common set of standardized questionnaires used by healthcare professionals to evaluate the condition of patients with osteoarthritis of the knee. The WOMAC includes questions relating to pain, stiffness, and the physical functioning of the joints.

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On the degenerative disk disease and senescent cells from FightAging: “… It is just a pity that so few older people know this at the present time — the hundreds of millions worldwide who are suffering when perhaps they need not be…”

At this point, I suspect it will surprise no-one who follows the field to learn that the accumulation of senescent cells is a significant cause of degenerative disc disease. The evidence from a mouse study that is provided in the open access paper here doesn’t quite rise to establishing that claim, but it is compelling nonetheless. Given the role of cellular senescence in arthritis, a disease of localized chronic inflammation, it is logical to also expect a role in the degeneration of intervertebral discs, as this is also a condition of aging in which inflammation seems important.

Senescent cells, even while present in only comparatively small numbers, generate a potent mix of molecules that spurs chronic inflammation and is destructive of surrounding tissue structure. Fortunately early senolytic compounds, those shown to destroy a sizable fraction of senescent cells cells in animal studies, are cheap and readily available to anyone willing to try this self-experiment. It is just a pity that so few older people know this at the present time — the hundreds of millions worldwide who are suffering when perhaps they need not be.

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Topol is a dreamer. “One can imagine that AI will rescue medicine from all that ails it, including diagnostic inaccuracy,” he writes. (There are roughly 12 million misdiagnoses of serious illness in the United States every year, and medical error kills a quarter-million Americans annually.) But even Topol admits that this hope is far from being actualized. Indeed.

Cardiologist Eric Topol explores the benefits of artificial intelligence in medicine.

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A new story on my latest article from #transhumanism critic Wesley J. Smith:

Oh my. Two of contemporary society’s most prominent anti-human utopian movements — radical environmentalism and materialistic transhumanism — appear on the verge of a bitter showdown.

When you think about it, that makes sense. Both movements see themselves as the future’s only hope. But their core purposes are incompatible. Radical environmentalists — “nature rights” activists, deep ecologists, Gaia theorists, and their fellow travelers that elevate nature above humanity — hijacked and refashioned traditional environmentalism into a mystical neo-earth religion that disdains homo Sapiens as a parasitical species afflicting the earth. These radicals hope to thwart our thriving off the land in order to “save the planet.” Indeed, I sometimes believe that if they could, they would forcibly revert our species to hunter/gatherers — without the hunting part.

In contrast, transhumanism denigrates both the natural world and normal human life as irredeemably limited, and worst of all, ending in death! They yearn to possess extraordinary capacities without having to work to attain them. Rather than pursue virtue, transhumanism expects to overcome human nature through applied technology. Indeed, movement prophets predict the coming of “Singularity” — a discreet moment in time when unstoppable cascading technology will enable transhumanists to “seize control of human evolution” and reengineer themselves into an immortal “post-human species.”

The intellectual peace between these competing social movements was recently breached by Zoltan Istvan, one of transhumanism’s most creative apologists, who ran for president in 2016 on a plank of defeating death and garnered scads of earned media by touring the country in a bus fashioned to look like a coffin. In an all-out frontal assault on the hallowed presumption of contemporary environmentalism, Istvan not only writes that “nature isn’t sacred” (can you hear the gasping?), but he committed an even worse anti-environmentalist sin by arguing that “we should replace it.”

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Bacterial cells that normally colonize our guts can distinguish themselves from other bacterial species using what’s traditionally considered their enemy—a virus. Researchers report April 16 in the journal Cell Reports that some bacteria use viruses that have infected them (i.e., phages) for self-recognition and thereby show greater fitness, repelling competitors that lack this adaptation.

This is the first evidence that cells can distinguish themselves from related competitors through the use of a virus. The implications are that we should re-evaluate the relationship between a virus and its cellular host in that there are sometimes benefits to having a viral infection.”

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